Treatment of comorbid COPD and CHF. Chronic obstructive pulmonary disease and comorbidities. COPD and lesions of the cardiovascular system. Results and discussion

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Seminar "Chronic obstructive pulmonary disease in combination with chronic heart failure: complex issues of diagnosis and treatment"

Conducts: Republican Medical University

The date of the: from 25.09.2014 to 25.09.2015

Chronic obstructive disease (COPD) and chronic heart failure (CHF) are characterized by high prevalence, morbidity (morbidity is any deviation, objective or subjective, from the state of physiological or psychological well-being) and mortality, and therefore represent a serious medical and social problem. In the last two or three decades, significant progress has been made in studying their prevalence, etiology, pathogenesis, and determining therapeutic approaches.

A very limited number of studies have been devoted to studying the prevalence, features of the course and prognosis, as well as the effectiveness of various treatment regimens in patients with a combination of COPD and CHF. In this regard, a number of important issues remain insufficiently studied, including the diagnosis of COPD in patients with CHF and vice versa; the true incidence of COPD and CHF comorbidity, the impact of such comorbidity on the prognosis and selection of adequate treatment programs [1-6]. It should be noted that in the Recommendations of the European Association of Cardiology for the diagnosis and treatment of acute and chronic heart failure (2012) and the GOLD (Global initiative for the diagnosis and treatment of COPD) review 2013, undeservedly little attention is paid to the features of diagnosis, treatment and prognosis, respectively, in patients with CHF and concomitant COPD, and in patients with COPD in the presence of CHF [ , ].

Terminology, epidemiology, prognosis.

It may be considered appropriate to give definitions of COPD and CHF, presented in modern consensus documents. “COPD is a common disease characterized by persistent airway restriction (bronchial ostrusion), usually progressive, and associated with inflammation in the airways in response to harmful particles or gases (primarily due to smoking). Exacerbations and concomitant diseases make a significant contribution to the severity of the course of the disease. CHF is defined as a condition accompanied by a violation of the structure and function of the heart, in which it is not able to provide the release into the circulation of such an amount of oxygenated blood that would satisfy the needs of the tissues. From a clinical point of view, CHF is a syndrome characterized by decreased exercise tolerance, fluid retention, progressive nature, and limited life expectancy.

It is rather difficult to estimate the true prevalence of the combination of CHF and COPD in clinical practice, which is explained by a number of reasons. First, cardiologists responsible for the diagnosis and treatment of CHF pay insufficient attention to the assessment of lung function, which is why the incidence of detection of concomitant COPD remains low. Conversely, pulmonologists, who are engaged in the diagnosis and treatment of patients with COPD, underestimate the likelihood of concomitant CHF and do not perform appropriate diagnostic measures. Second, both CHF and COPD share a significant commonality of risk factors, symptoms, and physical findings. Thirdly, instrumental confirmation of the diagnosis can also be difficult, in particular, emphysema and pulmonary hyperinflation often make it difficult to conduct an echocardiographic (EchoCG) study, and significant congestion in the pulmonary circulation is often accompanied by the development of obstructive changes in spirometry. Large-scale epidemiological studies that assessed the true prevalence of the combination of COPD and CHF in the general population have not been conducted. Traditionally, the prevalence of these comorbidities was assessed separately: only in the contingent of patients with CHF or only in individuals with COPD.

According to a large-scale meta-analysis, which included dozens of observational studies with a combined population of more than 3 million people, the prevalence of COPD worldwide is about 7%. Annual mortality from COPD in the general population is relatively low (about 3%), but very high after hospitalization due to exacerbations (25%) [10-12]. Experts from the World Health Organization (WHO) and the World Bank in the study of the Global Burden of Disease predict that in 2030 COPD will take 3-4th place in the overall structure of mortality worldwide.

CHF is less common compared to COPD, and occurs in 1-3% of people in the general population [14-17]. However, CHF is associated with a distinctly negative prognostic indicator. Annual mortality in the general population is approximately 5-7%, the average life expectancy after hospitalization for decompensation of the disease is less than 2 years [18-20].

The detection rate of COPD in patients hospitalized for CHF ranges from 9 to 51% in different studies [ , ]. Along with this, in outpatients with stable CHF, it is detected with a frequency of 7-13%. This difference can be explained by the fact that “pseudo-obstructive” spirometric changes develop during CHF decompensation, which resolve after adequate CHF therapy.

On the contrary, characterizing the prevalence of CHF among patients with COPD, it can be noted that for quite a long time CHF was assigned a place mainly as a complication of severe COPD in the form of the development of right ventricular CHF, i.e. cor pulmonale. Such ideas were based mainly on the results of several small studies performed in the 70s of the twentieth century in relatively young patients with severe COPD without concomitant coronary heart disease, and, accordingly, left ventricular dysfunction. Only recently enough data has been accumulated that convincingly demonstrates the high prevalence of CHF in COPD (about 25%) [22-24]. At the same time, the dominant place in its origin is given to dysfunction of the left ventricle (LV), while the role of pulmonary hypertension and cor pulmonale in the development of CHF in COPD is important, but not of paramount importance [25-27].

In general, summarizing the data on the epidemiology of the combination of CHF and COPD, we can formulate a kind of “rule”: every fifth patient with CHF has concomitant COPD, and every fourth patient with COPD has CHF.

Pathogenetic mechanisms of interaction between COPD and CHF.

The relationship between COPD and the cardiovascular system is far from being fully understood. It is believed that the commonality of risk factors (smoking, older age), as well as the presence of systemic inflammation in both diseases, plays a key role in the overall pathophysiology of COPD and CHF. In particular, most patients with severe COPD have a 2–3-fold increase in circulating C-reactive protein levels, which is one of the most important markers of systemic inflammation [28–30]. One hypothesis that explains the higher prevalence of LV systolic dysfunction in COPD patients is that systemic inflammation accelerates the progression of coronary atherosclerosis and coronary heart disease. In addition, circulating pro-inflammatory mediators may have a direct cytotoxic effect on myocardiocytes, and thus stimulate the progression of myocardial dysfunction [31–33].

In addition to the systemic consequences of smoking and inflammation, COPD and CHF have other common mechanisms that cause the mutual progression of the disease. Both diseases are accompanied by hyperactivation of the renin-angiotensin system (RAS). Angiotensin II is a powerful bronchoconstrictor that can activate lung fibroblasts and stimulate apoptosis of lung epithelial cells, as well as increase pulmonary hypertension and impair gas exchange through the alveolar-capillary membrane [ , ]. COPD is also accompanied by excessive activity of the sympathetic system, which plays an extremely important role in the progression of CHF [,]. Both diseases equally affect cellular metabolism, stimulating the replacement of glucose-dependent energy processes with lipid-dependent ones, resulting in progressive muscle dysfunction and loss of muscle mass with the development of cachexia in the final cascade of both diseases [ , ].

Probably the most important pulmonary effects of CHF are increased pulmonary herniation capillary pressure, pulmonary congestion, and the presence of interstitial and peribronchiolar edema. These phenomena can lead to a decrease in the diffusion capacity of the lungs and stimulate remodeling of the pulmonary vascular bed with the development of hypertrophy of the walls of the pulmonary arterioles [ , ]. In addition, a secondary increase in pulmonary artery pressure may develop due to LV dysfunction. On the other hand, the alveolar hypoxia inherent in COPD and, as a result, pulmonary vasoconstriction additionally enhance the remodeling of the pulmonary vascular bed due to: 1) redistribution of blood flow from insufficiently ventilated areas to better ventilated areas of the lungs; 2) additional hypertrophy of the walls of the pulmonary arteries; 3) proliferation of vascular smooth muscle cells in those vessels of the pulmonary circulation, which normally should not be muscular [ , ]. With a corresponding lesion of a significant part of the lungs, increased pulmonary vascular resistance and pulmonary arterial hypertension develop, which thus leads to an increase in the load on the right ventricle and can lead to dilatation and hypertrophy of the right ventricle and, finally, insufficiency of the right heart (cor pulmonale) [ , 38-42].

Are common questions diagnostics combinations COPD And CHF.

Often, the correct diagnosis and differential diagnosis of COPD and CHF are associated with certain difficulties and require various laboratory and instrumental studies. The following summarizes the main diagnostic and differential diagnostic features that are used in the diagnosis of COPD in the presence of concomitant CHF.

Clinical manifestations of COPD and CHF are very similar [ , , , ]. Dyspnea on exertion is the main complaint in both conditions. In most cases, with both diseases, mixed dyspnea occurs, in patients with CHF, often with a predominance of the inspiratory component, and in COPD, the expiratory component. Patients with CHF may experience orthopnea, which is not characteristic of COPD. An important symptom characteristic of CHF is paroxysmal nocturnal dyspnea, which is usually clearly reduced in an upright position, which can serve as a differential sign with asthma attacks, sometimes observed in COPD. Increased fatigue is also very characteristic of both diseases. Cough, both with sputum production and dry, is predominantly found in COPD, however, it is not uncommon in severe CHF. Episodes of acute cardiac decompensation can lead to the development of pulmonary obstruction with wheezing and prolongation of exhalation, which are sometimes difficult to distinguish from attacks of bronchospasm. Depressive and anxiety symptoms are very common both in patients with COPD and in patients with CHF.

Objective examination of the heart and chest is usually difficult due to the presence of pulmonary hyperinflation, and therefore has neither sufficient sensitivity nor specificity. In patients with severe COPD, the chest acquires a characteristic emphysematous (“barrel-shaped”) shape, and a box sound is observed during percussion, which is not typical for patients with CHF. In CHF with a reduced left ventricular ejection fraction, the first tone is usually significantly weakened, a proto- and or presystolic gallop rhythm and blowing pansystolic murmur are often heard, which is not characteristic of most patients with COPD.

Plain chest radiography is not a sensitive method for diagnosing the combination of COPD and CHF. On the one hand, emphysema and/or hyperinflation of the lungs can mask and reduce the shadow of the heart, reducing the value of the cardiothoracic index. In addition, COPD-specific pulmonary vascular remodeling and areas of changes in the density of the lung tissue can both mask and mimic the phenomena of congestion and interstitial pulmonary edema. However, plain radiography is an important and useful method for detecting other important pathology localized in the chest cavity. In particular, it remains an important screening method, playing an auxiliary, but very significant role in the diagnosis of CHF.

X-ray symptoms in favor of the presence of CHF are considered to be an increase in the cardiothoracic index> 0.50, signs of redistribution of blood flow in the lungs (increased vascular pattern and enlargement of the caliber of veins in the upper lobes of the lungs, possibly a slight expansion of the root and an increase in the caliber of orthogonal vascular shadows in the central parts of the lungs), signs of interstitial edema (intensification of the pattern, polymorphic pattern, cellular deformation of the pattern, blurred blood vessels and bronchi, the presence of Kerley lines, pleural lines) and alveolar edema (multiple confluent focal shadows due to the accumulation of transudate in the alveoli). It has been proven that a careful analysis of plain chest radiographs in patients with exacerbation of COPD can not only significantly improve the diagnosis of the presence of concomitant CHF, but also establish a group of patients with a negative survival prognosis.

DiagnosticianA COPD in the presence of comorbid CHF.

Approaches to the diagnosis of COPD in the presence of concomitant CHF are generally the same as in patients without comorbidity. The above definition of COPD identifies two fundamental aspects inherent in COPD: firstly, persistent (i.e., permanent and not fully reversible) bronchial obstruction, and secondly, the association with pathogenic inhalation exposure. Thus, their presence is necessary and mandatory for a correct diagnosis. According to the recommendations of the Global Initiative for Chronic Obstructive Lung Disease (GOLD 2014), the diagnosis of COPD should be considered in all patients over 40 years of age with characteristic clinical manifestations exposed to risk factors. It can be separately noted that in the assessment of inhalation risk factors, smoking dominates (more than 10 pack-years, more often 20-30 pack-years), which is a direct etiological factor in the development of COPD in at least 75-80% of patients. In the remaining 20-25% of patients with COPD, the main causative exposure is household and industrial pollution (usually fossil fuel combustion products) and/or occupational inhalation pollution. In patients older than 40 years who present characteristic complaints and have been exposed to inhaled risk factors, the probability of having irreversible bronchial obstruction is about 30-40%. Such patients must necessarily perform a spirometric study to verify the diagnosis.

Spirometry study function of external respiration is the most important and mandatory stage in the diagnosis of COPD. A mandatory diagnostic criterion, without which the diagnosis of COPD is impossible, is confirmation of the presence of incompletely reversible bronchial obstruction. By incompletely reversible bronchial obstruction is understood obstruction, which, after the use of a high dose of bronchodilators (usually 400 micrograms of salbutamol), does not completely resolve, regardless of the degree of increase in ventilation function indicators. Usually, spirometry is used to determine the presence of reversibility of obstruction, in which the ratio of forced expiratory volume in the first second (FEV 1) to forced vital capacity (FVC) is calculated.

The criterion for incompletely reversible obstruction is the persistence of the FEV 1 / FVC ratio after a test with a bronchodilator less than a certain threshold value (diagnostic criterion) [ , ]. However, despite the significant efforts of international and national expert groups and professional associations, there is still no consensus on a single spirometric criterion for bronchial obstruction, and, accordingly, the functional diagnosis of COPD.

The most commonly used spirometric criterion for bronchial obstruction, proposed in the GOLD Guidelines, is the ratio of FEV 1 / FVC<0,7 (так называемый фиксированный критерий) . Его основным преимуществом является простота вычисления, однако ему присущи существенные ограничения, потому что он не принимает во внимание физиологический феномен возрастного снижения легочной функции, следствием чего является высокая частота гипердиагностики ХОБЛ у пожилых лиц и недостаточная диагностика обструктивных изменений у молодых. Зато в общих рекомендациях Американского торакального общества и Европейского респираторного общества (American Thoracic Society / European Respiratory Society (ATS/ERS 2005)) предлагается использование критерия, основанного на популяционных статистических расчетах (нижняя граница нормы, lower limit of normal – LLN) . Он сложнее вычисляется, однако его основное преимущество в том, что он является абсолютно традиционным для расчета любых норм в медицине вообще. Как и в случае нормы почти любого лабораторного или инструментального показателя, 95% относительно здорового населения имеет ОФВ 1 /ФЖЕЛ больше, чем LLN. Поэтому данный показатель лишен риска ложно-положительной диагностики ХОБЛ в старшей возрастной группе и ложно-отрицательной диагностики у молодых лиц. LLN не представлен тем или другим цифровым значением, так как сильно зависит от пола, этнической принадлежности, роста, и, главное, возраста. Чтобы наглядно проиллюстрировать взаимоотношения фиксированного критерия ОФВ 1 /ФЖЕЛ<0,7 и статистически обоснованного ОФВ 1 /ФЖЕЛ

Rice. 1. Comparison of the fixed criterion FEV 1 / FVC<0,7 и LLN, в зависимости от возраста и роста у мужчин европейской этнической принадлежности.

As you can see, FEV 1 / FVC<0,7 (обозначен красной пунктирной линией), не зависит от демографических показателей больного, в то время как соответствующие значения ОФВ 1 /ФЖЕЛ и LLN (изогнутая плоскость серого цвета) существенно и нелинейно меняются с изменением возраста и роста. В данном случае график построен с учетом одинакового пола и этнической принадлежности (у мужчин белой расы). Если же учитывать гетерогенность этих параметров, то указанная на рисунке плоскость имеет еще более нелинейный характер, что делает несоответствие LLN фиксированному критерию 0,7 особенно подчеркнутой.

It has been established that, in contrast to the fixed criterion FEV 1 / FVC arbitrarily chosen by experts<0,7, использование ОФВ 1 /ФЖЕЛ

The choice of the optimal diagnostic criterion is especially relevant in the context of COPD in combination with CHF, since both of these diseases are more common in the elderly. In addition, pulmonary congestion, cardiomegaly, pleural effusion, and other phenomena inherent in CHF can additionally change spirometric parameters, complicating the diagnosis and assessment of the severity of COPD. In particular, during the decompensation of CHF, approximately 20% of patients develop "pseudo-obstructive" spirometric changes with a significant decrease in FEV 1 / FVC. After the appointment of diuretic therapy, these phenomena are independently resolved without the use of bronchodilators. Preliminary evidence has now been published on the benefit of using FEV1/FVC

In contrast to the actual diagnosis of bronchial obstruction, the criteria for assessing its severity in patients with COPD are consistent and almost not discussed. In previous versions of the GOLD guidelines (until 2011), a gradation was proposed and widely used based on the assessment of post-bronchodilation FEV 1: FEV 1 ≥ 80% - mild obstruction; at 50% ≤ FEV 1<80% – среднетяжелая обструкция; при 30% ≤ ОФВ 1 <50% – тяжелая обструкция и при ОФВ 1 <30% – очень тяжелая обструкция. Однако эти градации с 2011 года фактически имеют описательный или научный, но не практический интерес, так как в новой редакции GOLD (с 2011 года) эксперты фактически оставили 2 категории – тяжелая и нетяжелая (ОФВ 1 менее и более 50%, соответственно). Классификация заболевания и выбор тактики лечения базируются только на таком распределении.

Despite widespread use, an approach to assessing the severity of obstruction based on the calculation of percent predicted FEV 1 potentially has the same disadvantages as using a fixed criterion of obstruction compared to LLN. First, it is based on the false premise that a given percentage of what should be is equivalent for all individuals, regardless of age, height, gender, or ethnicity. The discrepancy between this premise and the truth can be illustrated by an example: LLN for FEV 1 in a man of average height at the age of 30 years can be 74% of the due, and at the age of 70 63% of the due. Second, all of the above cut-off points for the distribution of severity categories are arbitrarily chosen based on expert opinion. The result of these shortcomings of the traditional approach to assessing the severity of obstruction may be an underestimation of the severity of pulmonary ventilatory dysfunction in young people and, which is especially important for patients with COPD and CHF, an overestimation in the elderly.

bronchodilation test. According to the established tradition, for more than half a century, one of the key signs that distinguish between COPD and bronchial asthma (BA) has been considered the reversibility of bronchial obstruction under the influence of bronchodilators. Currently, the study of obstruction reversibility using a bronchodilatory test (BDT) has become firmly established in clinical practice and is regulated by modern consensus documents in the diagnosis of both BA and COPD [ , ]. However, back in the 80s of the last century, the differential diagnostic value of BDT was subjected to justified criticism. Test results are highly dependent on many uncontrollable factors (drug, dose, natural response variability, various standards, and others). This leads to frequent cases of misdiagnosis, which leads to inadequate therapy and adverse patient outcomes.

It is very difficult to give an unambiguous definition of the term "reversibility of bronchial obstruction". Firstly, this is due to the use of different criteria in various clinical guidelines, and secondly, to the difficulties of adapting generally accepted English terms. In particular, the analogue of the most widely used concept - "bronchodilator reversibility" - is the Russian term "reversibility of bronchial obstruction". This term carries a certain duality. On the one hand, they speak of reversible obstruction with complete resolution of obstructive phenomena (if, after the use of a bronchodilator, FEV 1 / FVC becomes more than 0.7 or LLN). On the other hand, the concept of obstruction reversibility is also used to describe a significant increase in spirometric parameters after bronchodilation. In the GOLD 2014 recommendations, FEV1 increase after bronchodilation by ≥ 12% and ≥ 200 ml is considered significant. In the ATS / ERS 2005 recommendations, in addition to FEV 1, reversibility can also be assessed by the FVC indicator (the same numbers).

As an illustration of the conflicting manifestations of the same term, one can give an example of mild obstruction, which was completely resolved after BDT, but the increase in FEV 1 was only 4% and 110 ml. In this case, the criteria for both "reversible" and "irreversible" obstruction are met. To avoid such terminological conflicts, in foreign literature, the concept of “bronchodilator responsiveness” is often used to describe the increase in lung volumes and flows, which can be referred to as “response to a bronchodilator” [ , ]. Thus, the results of RDT allow us to describe two parameters: the reversibility of bronchial obstruction (reversible / not reversible) and the response to a bronchodilator (pronounced / not expressed).

All current international guidelines regarding spirometry state that the presence of a pronounced response to a bronchodilator is not a sufficient diagnostic criterion for diagnosing asthma, as was previously believed. This is due to a number of factors.

First, a pronounced response to a bronchodilator is often observed in patients with "pure" COPD, without concomitant asthma. Indicative are the results of a large-scale UPLIFT study, in which a pronounced response to a bronchodilator was observed in about 40% of patients with COPD.

Secondly, the “reversibility” of bronchial obstruction is an unstable characteristic, variable over time. In a study by P.M. Calverley et al. (2003) the status of "reversibility" of obstruction repeatedly changed in half of patients with COPD during 3 months of follow-up. A similar multiple change in "reversibility" was also demonstrated in patients who are traditionally considered the least prone to the action of bronchodilators - in 13% of patients with emphysema.

Thus, when evaluating a patient with suspected COPD, the main diagnostic value of the use of RDT is to improve the quality of COPD diagnosis by excluding cases of completely reversible obstruction (usually due to the presence of asthma).

Diagnosis of CHF in the presence of comorbid COPD.

According to the recommendations of the European Society of Cardiology (2102), the diagnosis of CHF is based on an assessment of the presence of subjective symptoms and objective signs of CHF and objective evidence of the presence of structural and functional lesions of the heart (systolic and/or diastolic dysfunction, dilatation and/or hypertrophy of the heart chambers), obtained using an instrumental study (first of all - echocardiography). An auxiliary criterion is also a positive clinical response to CHF treatment.

There are two main variants of CHF: with reduced LV systolic function (ejection fraction (EF) of the LV<40%) и с сохраненной систолической функцией ЛЖ (фракция изгнания (ФВ) ЛЖ>40%). To establish the first option, it is necessary to have: (1) characteristic complaints (2) objective data inherent in CHF; (3) a confirmed decrease in LVEF. Installing the second option requires (1) complaints; (2) objective data inherent in CHF; (3) confirmed preserved LV systolic function in the absence of LV dilatation; (4) the presence of LV hypertrophy/dilatation of the left atrium and/or echocardiographic evidence of the presence of diastolic dysfunction (preferably based on tissue Doppler sonography).

It should be noted that the diagnostic criteria presented in the above recommendations are not discrete, but probabilistic in nature (in the categories “reduces the likelihood” or “increases the likelihood” of a diagnosis) and in many cases does not provide a basis for an unambiguous interpretation of the totality of clinical data. In the presence of concomitant COPD, the accurate diagnosis of CHF (especially the variant with preserved LV systolic function) becomes especially difficult.

Echocardiography in patients with COPD may be difficult due to the presence of a poor acoustic window due to the presence of hyperinflation of the lungs. The incidence of inadequate imaging depends on the severity of COPD, and, according to a number of studies, is 10%, 35%, and more than 50% in individuals with mild, severe, and extremely severe COPD, respectively [ , , 57-59]. A normal echocardiographic picture makes it possible to completely exclude the presence of CHF. Detection of the left ventricular ejection fraction (LVEF)< 40% позволяет говорить о ХСН со сниженной ФВ ЛЖ. Постановка диагноза ХСН с сохраненной ФВ ЛЖ (при ФВ ЛЖ >40% and the presence of chamber dilatation and/or LV myocardial mass increase and/or evidence of LV diastolic dysfunction) is a challenging issue even in the absence of comorbid COPD. And the presence of this comorbidity may further complicate the assessment of both symptoms and data from all laboratory and instrumental methods of investigation.

The study of the levels of BNP and NT-proBNP is useful to rule out CHF in individuals with acute or worsening dyspnea. The criterion that allows 98% to exclude the presence of CHF is low levels of these peptides (NT-proBNP< 300 пг/мл или BNP < 100 пг/мл). У больных ХОБЛ уровни BNP от 100 до 500 пкг/мл могут свидетельствовать о наличии правожелудочковой недостаточности, левожелудочковой недостаточности или о сочетании обоих вариантов. Уровни BNP >500 pg/ml in a symptomatic patient can be considered as a sign of acute heart failure, which should lead to the initiation of appropriate treatment. However, it should be remembered that natriuretic peptides are often false positive, i.e. have low specificity and positive predictive value, and thus play only an auxiliary role in confirming the diagnosis of CHF. This observation is especially relevant in the presence of concomitant COPD, since the diagnostic properties of natriuretic peptides have been very limitedly studied in such patients.

Violation of the structure and function of the left ventricle in patients with COPD. By the beginning of the 2000s, the symptoms of CHF in a patient with COPD were traditionally considered a sign of insufficiency of the right heart (cor pulmonale). This stereotype was based on data from a number of small studies of COPD and CHF comorbidity published in the 1970s and 1980s, which included relatively young patients (mean age 53–68 years) with severe COPD and, importantly, without concomitant coronary heart disease. Clinically significant LV dysfunction was observed in 0-16%. Based on this, the idea dominated for a long time that in patients with COPD with signs of CHF, left ventricular dysfunction does not play a significant role, however, in 2003 P.A. McCullough et al. and later in 2005 F.H. Rutten et al. found that every fifth patient with COPD has undiagnosed left-sided CHF [ , ]. Subsequently, much evidence has accumulated that in real clinical practice, COPD patients very often have undiagnosed LV hypertrophy (in 43.2% of women and 21.4% of men, respectively), as well as systolic and diastolic LV dysfunction (in 22% and 71% of cases, respectively) [ , , 63-71]. Gradually, the academic community came to the conclusion (and now it dominates) that impaired LV structure and function are the key factors in the development of CHF symptoms in the vast majority of COPD patients, including because concomitant cardiovascular diseases are the most common COPD comorbidity (before 70% of patients).

The above, of course, does not exclude the role of structural and functional changes in the pancreas both in the development of symptoms of overload of the systemic circulation, and in the deterioration of LV function through the inherent mechanisms of interventricular interaction [ , , , ]. In addition, there are a number of factors that simultaneously negatively affect the work of both the left and right heart. For example, pulmonary hyperinflation, especially during physical exertion, has the effect of compression of both ventricles, which leads to a decrease in diastolic filling, a decrease in stroke volume and cardiac output [ , , , ]. On the other hand, during exacerbations of COPD, decompensation of right ventricular dysfunction is often observed, which leads to the development or intensification of systemic congestion and peripheral edema. It should be noted that such episodes are not always accompanied by an increase in mean pressure in the pulmonary artery system, which proves the role of other factors in the genesis of the decrease in RV contractility. Moreover, exacerbations of COPD are often accompanied by the appearance of peripheral edema, even without signs of RV decompensation due to hypercapnia and respiratory acidosis, which are accompanied by sodium retention and fluid retention.

The role of chronic cor pulmonale and pulmonary hypertension in the evaluation of a COPD patient with CHF symptoms. In 1963, WHO experts gave the following definition of chronic cor pulmonale (CHP): “Cor pulmonale is hypertrophy of the right ventricle that develops as a result of diseases that impair the function and / or structure of the lungs, with the exception of cases where pulmonary changes are the result of primary lesions of the left heart or congenital heart defects". Despite the fact that the concept of "cor pulmonale" is very popular in clinical practice, the given definition is pathomorphological rather than clinical, and is not well suited for clinical use, resulting in a very broad and heterogeneous interpretation of this concept. Considering that pulmonary hypertension (PH) is a key phenomenon in the development of cor pulmonale, and it is the diagnosis and treatment of various types of PH (not only associated with lung diseases) that is emphasized in most modern international consensus documents, many experts consider the definition of CHLS given by E Weitzenblum (2003): "CHLS is the consequences of PH caused by diseases affecting the structure and / or function of the lungs, in the form of hypertrophy and / or dilatation of the right ventricle (RV) of the heart with symptoms of right-sided heart failure" .

PH is a common complication of COPD, although the increase in pressure in the pulmonary artery system is usually mild to moderate. For patients with non-severe obstruction, an increase in pulmonary artery pressure is atypical, and in COPD with FEV 1<50% частота клинически значимой ЛГ с развитием симптомов может достигать 5-10%. Распространенность клинически значимых проявлений ХЛС составляет 2-6 случаев на 1000 человек, а количество ежегодно регистрируемых новых случаев ХЛС – 1-3 на 10 000 человек.

It should be noted that if earlier in the development of CLS the main role was assigned to chronic hypoxemia with the development of PH, subsequent overload of the pancreas and the formation of right ventricular failure and stagnation in the systemic circulation, then in recent years this concept has been the subject of increasing debate. In particular, it has been shown that a significant number of COPD patients with clinically significant congestion have only minor PH with relatively preserved structure and function of the pancreas. In this regard, the development of CLS symptoms (especially edematous syndrome) is mainly explained by hypercapnia, associated systemic vasodilation, activation of neurohumoral systems, and sodium and water retention by the kidneys. Therefore, for the diagnosis of CLS, the assessment of clinical symptoms has low sensitivity and specificity, and the basis for verifying the diagnosis is the study of the structure and function of the pancreas and the state of the pulmonary circulation.

The most commonly used method in routine practice for assessing PH and structural and functional changes in the pancreas is echocardiography. In particular, in the general population, Doppler-assessed LH levels have been shown to be highly correlated with invasive pulmonary artery pressure levels. But, unfortunately, patients with COPD are an exception to this rule. First, the hyperinflation of the lungs inherent in COPD makes it impossible to adequately visualize the heart in half of patients with severe disease, that is, in those who have more frequent CLS. Secondly, the average error in estimating pulmonary artery pressure using Doppler ultrasonography compared to the invasive "gold standard" is about 10 mmHg. . In a large study (n = 374) of candidates for lung transplantation (primarily due to COPD), systolic pressure in the pulmonary artery using Doppler ultrasound could only be assessed in 44% of patients, and of these, in 52% of cases, the estimates were significantly incorrect compared to invasive estimate (difference > 10 mmHg). In addition, it should be added that in any international clinical guidelines for the diagnosis of PH, only indicators obtained during cardiac catheterization (mean pulmonary artery pressure> 25 mm Hg) are used.

Due to the lack of accuracy in assessing pulmonary artery pressure based on echocardiography, the experts of the Working Group of the European Society of Cardiology and the European Respiratory Society on the diagnosis and treatment of PH in their general recommendations indicate that the diagnosis of PH can only be determined at the level of systolic pressure in pulmonary artery> 50 mm Hg, i.e. at least twice the usual diagnostic threshold. It is traditionally believed that the main benefit of echocardiography in the diagnosis of PH is its high negative predictive value, that is, it allows you to exclude the presence of PH with high confidence at low pressures in the pulmonary artery, but requires additional verification by cardiac catheterization at high pressures in the pulmonary artery. pulmonary artery. It also deserves attention that high levels of mean pressure in the pulmonary artery (more than 40 mm Hg during invasive examination) are quite atypical for COPD and always need to look for additional causative factors (obstructive sleep apnea, left ventricular dysfunction, pulmonary embolism, and others). ). Very rarely (1-3%) significant PH occurs in patients with non-severe COPD, in such cases it is called "disproportionate" PH. Patients with this variant of PH have mild obstruction, significantly reduced lung diffusivity, severe hypoxemia and hypocapnia, and are characterized by an extremely negative prognosis.

General approaches to the treatment of combined CHF and COPD.

Treatment of CHF in patients with COPD should be carried out in accordance with standard approaches. Most CHF patients with reduced LV EF are indicated for β-blockers. The use of selective β 1 -blockers (nebivolol, bisoprolol) is considered quite safe even with significant bronchial obstruction. It has been established that the use of β-blockers in patients with COPD can lead to some decrease in FEV 1 (especially when using non-cardioselective agents), but this phenomenon is not accompanied by an increase in dyspnea or a deterioration in the quality of life, and probably has no significant clinical significance [ , , ]. Moreover, observational studies and their meta-analyses have repeatedly demonstrated that patients who are constantly taking β-blockers have a lower incidence of COPD exacerbations, regardless of the degree of cardioselectivity of agents [81-84]. There is only one caution when using β-blockers in individuals with COPD. In a recently published large epidemiological study in people with extremely severe oxygen-dependent COPD, the use of β-blockers was associated with an adverse effect on prognosis. In general, for all other patients, the rule is true: the benefits of using selective β 1 -blockers in CHF significantly outweigh any potential risk.

In a number of small studies requiring further validation, angiotensin-converting enzyme inhibitors (ACE inhibitors) and angiotensin II receptor antagonists (ARA II), which are an obligatory component of the treatment of CHF with reduced LVEF, have been found to have a number of “pulmonary” effects beneficial in COPD. They are able to influence bronchial obstruction by reducing the levels of angiotensin II, improve alveolar gas exchange, reduce pulmonary inflammation and pulmonary vasoconstriction. Two recently published observational studies in patients with COPD showed a beneficial effect of ACE inhibitors and ARA II not only on cardiac endpoints, but also on a number of important pulmonary endpoints, such as COPD exacerbations, hospitalizations and respiratory mortality [ , ].

The use of statins is an integral component of the treatment of coronary heart disease, which is the most common cause of CHF. The presence of concomitant COPD does not affect the choice of lipid-lowering drug or its regimen. At the same time, based on the results of a number of studies, it has been established that the use of statins can have a beneficial effect on the course of COPD, reducing the frequency of exacerbations, hospitalizations, slowing the progression of lung function and reducing mortality [88-90]. However, these results were not confirmed in the only randomized STATCOPE trial to date, in which simvastatin 40 mg therapy was not associated with a reduction in the frequency of exacerbations compared with placebo.

Treatment of COPD in patients with CHF should be standard in accordance with international recommendations, since there is no convincing evidence that COPD in the presence of concomitant CHF should be treated differently. Special randomized studies of the efficacy and safety of COPD inhalation therapy in patients with CHF have not been conducted. Therefore, this expert recommendation is based mainly on the results of extensive studies in which long-term use of long-acting bronchodilators in patients both without CHF and with its presence not only did not increase the incidence of cardiovascular complications, but was also accompanied by a decrease in the risk of myocardial infarction and a number of cardiovascular events. events (fluticasone salmeterol in the TORCH study, tiotropium in the UPLIFT study) [ , ].

Along with this, the cardiovascular safety profile of some anticholinergic agents is currently being actively discussed, especially in the context of the development and/or decompensation of CHF. Several meta-analyses have shown that the short-acting anticholinergic ipratropium may increase the incidence and/or severity of CHF.

According to one study, in patients with CHF taking β 2 -agonists, there was an increase in the risk of mortality and the frequency of hospitalizations. It should be noted that the observational nature of this study does not allow a confident conclusion about the presence of relevant causal relationships. Therefore, there is no need to refrain from using this class of bronchodilators in CHF. But it may be worthwhile to more closely monitor patients with severe CHF receiving inhaled β2-agonists for COPD.

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The features of chronic heart failure (CHF) in patients with and without chronic obstructive pulmonary disease (COPD) were studied. For this purpose, 75 people were examined. The patients were divided into 2 groups based on the presence of COPD. The 1st group included 38 patients with COPD, the 2nd group included 37 patients without COPD. In patients with comorbidities, there is a decrease in exercise tolerance, aggravation of hypoxemia, an increase in heart rate, and higher systolic pressure in the pulmonary artery. An insufficient dosage of beta-blockers has been noted in patients with COPD, which can aggravate the course and progression of CHF. Thus, patients with COPD require special attention, a more detailed history taking and a thorough analysis of the data obtained for the timely diagnosis of cardiac pathology and the appointment of specific therapy, including highly selective beta-blockers.

chronic heart failure

chronic obstructive pulmonary disease

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Chronic heart failure (CHF) and chronic obstructive pulmonary disease (COPD) are the leading pathologies due to hospitalizations among elderly patients. Their combination potentiates systemic inflammation and hypoxia, which in turn lead to endothelial dysfunction, increased arterial stiffness, increased platelet reactivity, accelerated atherogenesis, apoptosis of myocardial and skeletal muscle cells. The presence of both pathologies in a patient is accompanied by an increased risk of adverse events in the form of recurrent myocardial infarction, more frequent decompensation of CHF and exacerbations of COPD. Death usually occurs from a cardiovascular cause.

The prevalence of CHF in Russia is 7% (7.9 million people). Clinically pronounced CHF occurs in 4.5% (5.1 million people). One-year mortality of patients is 12%, and three-year - 36%. . Terminal CHF reaches 2.1% of cases (2.4 million people). The prevalence of CHF in patients with COPD ranges from 7.2 to 20.9%, in the Russian Federation about 13%.

Timely diagnosis of CHF in patients with COPD allows the appointment of neurohumoral modulators, thereby improving the quality and life expectancy of patients.

Target

To study the features of CHF in patients with and without COPD.

Materials and methods

In accordance with the goal, 75 people with CHF were examined, hospitalized in the State Health Institution "Regional Clinical Hospital of Saratov" in the period from 2013 to 2014, who signed an informed consent to participate in the study. The study was approved by the Ethics Committee of the Saratov State Medical University. IN AND. Razumovsky" of the Ministry of Health of Russia. Inclusion criteria were male gender, age over 40 years and under 80 years, the presence of diagnosed CHF according to the recommendations of the Russian Society of Cardiology in 2013. The exclusion criterion was the presence of unstable coronary heart disease (CHD) (myocardial infarction, acute coronary syndrome) in less than 3 months before inclusion, heart defects, myocarditis, cardiomyopathies, acute and chronic diseases in the acute phase (with the exception of COPD). The patients were divided into 2 groups, depending on the presence of COPD. All patients underwent spirography using a MicroLab device (Micro Medical Ltd. (Great Britain), echocardiography using an Apogee`CX device using a 2.75 MHz probe with simultaneous recording of a two-dimensional echocardiogram and Doppler echocardiogram in a pulsed mode, N-terminal a fragment of the brain natriuretic peptide (BNP) using a kit of reagents manufactured by BIOMEDICA, Slovakia Clinical manifestations of CHF were assessed, the clinical status assessment scale for CHF (CHCS), the modified dyspnea scale (mMRC), the Charlson comorbidity index were used.

Statistical processing was carried out using the Statistica 8 package. To count features with a normal type of distribution, a t-test was used for independent groupings. For non-normal distribution, the Mann-Whitney test, the χ2 test with Yates correction were used. Correlation analysis was carried out. The difference in the indices of the groups at p<0,05.

results

Among the examined patients, 62 (83%) patients were in the cardiology department, of which 25 (40%) had COPD. COPD was diagnosed for the first time in 13 (21%) patients hospitalized in the cardiology department. Among those who had COPD previously diagnosed, the diagnosis was confirmed in all patients. Thus, there is an underdiagnosis of respiratory pathology at the prehospital stage, and the detection of COPD among patients with CHF corresponds to the literature data.

In 38 (50.7%) patients, COPD was diagnosed during spirography (group 2), and group 1 consisted of 37 patients without signs of COPD. As shown in Table 1, patients in both groups were comparable in age, frequency and duration of arterial hypertension, history of angina pectoris, body mass index.

Table 1

General characteristics of patients with and without COPD (M±s), (Me).

There were significantly more smokers among patients of group 2 than among patients of group 1 (p<0,001). Пациенты с ХОБЛ курили дольше (p>0.05) and more intense (p<0,001), чем больные с ХСН без ХОБЛ.

The duration of dyspnea as one of the main symptoms of COPD and CHF was comparable in patients with and without COPD. At the same time, the duration of cough as one of the main respiratory symptoms of COPD was longer in patients with respiratory pathology (p<0,001).

Patients with COPD and CHF had severe respiratory dysfunction. Most of the patients (60%) suffered from severe and extremely severe COPD.

Features of CHF in the studied groups of patients are presented in Table 2. In patients with comorbidity, such manifestations of CHF as edema in the lower extremities, hydrothorax are more often observed.

table 2

Features of manifestations of CHF in examined patients with and without COPD (M±s), (Me).

The problem of differential diagnosis of shortness of breath often has a difficult solution. The cause of shortness of breath can be a wide range of pathologies: heart and respiratory failure, anemia, obesity, etc. Of particular difficulty is the identification of heart failure in patients with COPD. This is mainly due to the presence of emphysema, which is able to hide such manifestations of CHF as moist, finely bubbling rales in the lungs, displacement of the percussion borders of the heart, and in some cases, a gallop rhythm. And bronchial obstruction, as a rather specific manifestation of COPD, can also be secondary, due to interstitial pulmonary edema. In this regard, spirography data in patients with severe cardiac decompensation are often not entirely objective, but the ratio of FEV 1 to FVC is more than 0.7 in the absence of COPD. Among the patients examined by us, this sign helped to exclude COPD in 7 (19%) patients of the 1st group.

To clarify the solution of the diagnostic problem, it is possible to identify clinical signs of decompensation in a patient with COPD in the form of manifestations of cardiac asthma - the inability to take a horizontal position, as well as swelling and pulsation of the jugular veins. When collecting an anamnesis, it is important to find out whether the patient is able to lie with a normal headboard during the interictal period. Among the patients of the 2nd group, manifestations of cardiac asthma were noted in 9 (24%) patients, and pulsation and swelling of the cervical veins were detected in 4 (11%) patients.

A decrease in physical performance was established (test with a six-minute walk) (p<0,001) и более выраженная гипоксемия (p<0,001) у пациентов с ХОБЛ и ХСН по сравнению с больными без респираторной патологии.

Currently, the result of a six-minute walk test is used to establish the functional class (FC) of CHF. According to our data, in the 1st group, the majority of patients (81.1%) had the 3rd FC of CHF, in 3 (8.1%) patients - the 2nd FC and in 4 (10.8%) patients - 4th FC. In the 2nd group, the 3rd FC also prevailed (76.3%), the rest were diagnosed with the 4th FC (23.7%).

At the same time, it should be taken into account that in patients with concomitant respiratory pathology, especially in severe and extremely severe COPD, the test result may be reduced due to broncho-obstructive disorders and the formation of respiratory failure. This may lead to overdiagnosis of CHF severity in patients with concomitant cardiorespiratory pathology. In this case, the necessary study is to determine the level of the N-terminal fragment of the BNP. Among patients with COPD, its level was 309 pg/ml.

In patients with COPD and CHF, an increase in heart rate (HR) was noted compared with patients without COPD. Currently, an increase in resting heart rate is associated with an increase in overall mortality, mortality from cardiovascular causes, the frequency of re-hospitalization due to cardiovascular causes, and exacerbation of CHF. A decrease in heart rate is associated with a reduced risk of death from cardiovascular causes, sudden death, and the likelihood of reinfarction. According to our data, in the majority of patients with COPD (61%), the heart rate was more than 80 beats per minute (p<0,001 с больными без ХОБЛ). Повышение ЧСС у больных с ХОБЛ и ХСН может быть связано с активным применением бронходилататоров этой категорией пациентов, а также с недостаточным назначением бета-адреноблокаторов либо использованием их в недостаточных дозах. Так, лишь 8 (21%) пациентов с сочетанием ХОБЛ, ХСН и перенесенного инфаркта миокарда (ИМ) постоянно получали бета-блокаторы, в то время как в группе без ХОБЛ таких пациентов было 20 (54%). Бета-блокаторы ранее рекомендовались 31 (83,8 %) больному 1-й группы и 22 (57,9 %) больным 2-й группы.

Among beta-blockers, all patients with COPD and CHF were prescribed bisoprolol at an average dose of 4.84±2.54 mg/day, with an average duration of administration of 4.57±4.96 years. In the group of patients without COPD, most patients also used bisoprolol (17-85%) at a dose of 4.79±2.25 mg/day. for 2.5±1.83 years), 1 patient received carvediolol at a dose of 12.5 mg/day. during the year, 1 patient - metoprolol succinate at a dose of 100 mg / day. for 3 years, 1 patient - nebivolol at a dose of 1.25 mg / day. during a year. There was no statistically significant difference in the dose and duration of taking bisoprolol in patients of both groups.

Among patients with CHF taking beta-blockers constantly, the average heart rate was 65.85±9.16 beats per minute, and in the group of patients with COPD and CHF - 75.77±10.2 beats per minute (p<0,01). Таким образом, у больных 2-й группы отмечена недостаточная дозировка бета-блокаторов, что, вероятно, связано с чрезмерной осторожностью врачей при назначении более высоких доз.

There were 17 (45%) patients with CHF and COPD who constantly took bronchodilators. Most often, patients in this group were prescribed berodual, which patients took for 1.82±1.07 years. Three patients constantly received formoterol at a dose of 24 mg/day. within 3.00±1.73 years. The average heart rate in patients constantly taking bronchodilators was 81.24±12.17 beats per minute.

When analyzing the features of myocardial infarction in patients with COPD and CHF, it turned out that the majority (34 patients, 90%) had an anginal variant, and 4 patients had a painless variant. In 25 (66%) patients, transmural changes in the myocardium were noted. Only one patient had a history of two MI, the rest - one at a time. The anterior wall was affected in 27 (71%) patients, the interventricular septum - in 22 (58%), the apex - in 21 (55%), the posterior wall was involved in the pathological process in 14 (37%) patients.

In the group of patients without COPD, 35 (95%) patients had an anginal variant, and 2 (5%) had an asthmatic variant. Transmural myocardial damage was found in 30 (81%) patients. 23 (62%) patients had one MI, 13 (35%) had two, and one patient had a history of three MIs. The anterior wall, interventricular septum, apex were affected in 26 (70%) patients, the posterior wall - in 19 (51%) patients.

Thus, transmural changes were stated equally often in the studied groups of patients. At the same time, in the COPD group, the presence of a painless form of MI was noted, which requires more careful attention of doctors to the management of this category of patients.

Detection of exertional angina in patients with COPD is rather difficult due to the fact that often the severity of shortness of breath does not allow patients to achieve the intensity of physical activity that can cause pain. As a rule, angina pectoris of a high functional class is diagnosed, which is also confirmed by our study, where out of 28 (74%) patients with an established diagnosis, 26 (93%) of them corresponded to the 3rd functional class, in one - to the 4th functional class, and only one - the 2nd FC. In the group of patients with CHF in the absence of COPD, angina pectoris was diagnosed in 31 (84%) patients, of which 26 (70%) - 3rd FC, 2 patients - 2nd FC and 3 patients - 4th FC .

According to modern concepts, the management of a patient with COPD, evaluation of the effectiveness of therapy and survival are largely determined by the frequency of exacerbation and its severity. Severe exacerbation is the main cause of death in patients. Each such episode is associated with an accelerated progression of the disease, a decrease in the quality of life, an increase in treatment costs, and decompensation of concomitant diseases, including CHF. Among the patients with COPD we examined, 12 (32%) had one exacerbation during the previous year, 11 (29%) patients had 2 exacerbations, three had 3 exacerbations, and one patient had a history of 4 exacerbations. At the same time, the exacerbation itself was the reason for hospitalization in 9 (24%) patients. The relationship between the frequency of exacerbations and FC CHF was noted (r=0.47, p<0,01), стадией ХСН (r=0,39, p<0,05), физической работоспособностью (r=-0,47, p<0,05), SaO 2 (r=-0,49, p<0,01), индексом BODE (r=0,52, p<0,01). Найденные взаимосвязи вероятнее всего обусловлены влиянием выраженности и тяжести патологического процесса в легких, усугубляющего течение и ускоряющего прогрессирование ХСН.

The ejection fraction (EF) of the left ventricle is one of the key indicators of hemodynamics in HF and has a great prognostic value: the lower the EF, the worse the prognosis. According to our data, in patients with COPD and CHF, the LV ejection fraction is significantly higher than in patients without COPD (p<0,05). Систолическая дисфункция левого желудочка (фракция выброса менее 35%) отмечалась у 6 (16%) пациентов с ХОБЛ и ХСН, у 7 (19%) больных без ХОБЛ. Фракция выброса менее 45% (используется в ряде исследований как показатель сниженной ФВ) имелась у 30 (81%) больных без ХОБЛ и у 20 (54%) пациентов с ХОБЛ и ХСН.

Patients with intermediate EF values ​​(from 35 to 50%) belong to the so-called gray zone, and they are recommended to be considered as having minor systolic dysfunction. There were 47 (62%) such patients in the group we examined: 26 (34%) patients had no signs of COPD, and 21 (28%) patients were diagnosed with COPD.

Normal ejection fraction (more than 50%) was detected in 4 (11%) patients without COPD and in 11 (29%) patients with COPD (p<0,001).

Systolic pressure in the pulmonary artery (SPPA) in patients with COPD and CHF significantly exceeds the level of the same indicator in patients without COPD (p<0,05). У пациентов с ХОБЛ и ХСН более высокий уровень легочной гипертензии может быть связан с сочетанными механизмами ее развития. При этом, учитывая сохранную фракцию выброса ЛЖ у большинства пациентов с ХОБЛ, значимый вклад вносит формирование легочной гипертензии в рамках хронического легочного сердца.

The causes of pulmonary hypertension are factors such as hypoxia, hypercapnia and acidosis, endothelial dysfunction. The latter may be associated with chronic hypoxemia leading to a decrease in the production of vasoconstrictors such as prostacyclin, prostaglandin E2, nitric oxide, as well as chronic inflammation.

Other factors that can lead to pulmonary hypertension include reduction in the area of ​​the capillary bed and compression of the pulmonary vessels associated with the destruction of the lung parenchyma in emphysema, as well as polycythemia, which can suppress endothelium-dependent vascular relaxation in response to acetylcholine.

When conducting a correlation analysis in patients with COPD, an inverse relationship was found between SPPA and exercise tolerance (test with a six-minute walk) (r=-0.40, p<0,05), сатурацией (r=-0,55, p<0,01) и прямая - с длительностью одышки (r=0,39, p<0,05) и количеством баллов по ШОКС (r=0,33, p<0,05). При оценке взаимосвязей СДЛА с параметрами Эхо-КГ была выявлена ожидаемая сильная прямая связь с размером правого предсердия (ПП) (r=0,80, p<0,001), конечным диастолическим размером правого желудочка (КДР ПЖ) (r=0,80, p<0,001), толщиной передней стенки правого желудочка (ТПСПЖ) (r=0,62, p<0,001).

Patients without COPD showed similar inverse relationships between SPPA and SaO 2 (r=-0.62, p<0,001), переносимостью физической нагрузки (тест с шестиминутной ходьбой) (r=-0,39, p<0,05) и прямые - с ШОКС (r=0,40, p<0,05), шкалой выраженности одышки mMRC (r=0,34, p<0,05), возрастом (r=0,40, p<0,05) и функциональным классом ХСН (r=0,39, p<0,05). Выявлены сильные прямые взаимосвязи с параметрами правых отделов сердца: с ПП (r=0,81, p<0,001), с КДР ПЖ (r=0,48, p<0,01), с ТПСПЖ (r=0,67, p<0,001).

conclusions

Diagnosis of CHF in patients with COPD is quite difficult, due to the similarity of the clinical picture of both pathologies, especially in the early stages of their development. In many ways, therefore, CHF is usually diagnosed in patients with severe and extremely severe COPD. Identification of low FC of angina pectoris in patients with COPD is also difficult due to the inability of patients to achieve the level of load that can lead to the appearance of pain. In patients with comorbidities, there is a decrease in exercise tolerance, aggravation of hypoxemia, an increase in heart rate, and a higher level of SPPA. More pronounced disturbances of some clinical and instrumental parameters are associated with an increase in pressure in the pulmonary artery. In patients of both groups, systolic dysfunction of the left ventricle (EF< 35%). При анализе проводимой терапии отмечена недостаточная дозировка бета-блокаторов у больных с ХОБЛ, что может усугублять течение и прогрессирование ХСН. Таким образом, больные с наличием ХОБЛ требуют особого внимания, более детального сбора анамнеза и тщательного анализа полученных данных для своевременной диагностики кардиальной патологии и назначения специфической терапии, в том числе и высокоселективных бета-блокаторов.

Reviewers:

Kosheleva N.A., Doctor of Medical Sciences, Associate Professor of the Department of Hospital Therapy, Faculty of Medicine, SSMU named after IN AND. Razumovsky, Saratov;

Nikitina N.M., Doctor of Medical Sciences, Associate Professor of the Department of Hospital Therapy, Faculty of Medicine, SSMU. IN AND. Razumovsky, Saratov.

Bibliographic link

We bring to your attention the journals published by the publishing house "Academy of Natural History"

Relevance. The combination of COPD and CHF leading causes of death common risk factors and pathogenetic mechanisms often combine, presenting diagnostic and therapeutic difficulties each is an independent predictor of morbidity, mortality each contributes to a decrease in the quality of life high costs of the healthcare system N. M. Hawkins, et al. European Heart Journal (2013) 34, 2795–2803

Definitions of CHF COPD is a violation of the structure or function of the heart, as a result of which the heart is unable to meet the body's need for oxygen at a normal filling pressure of the heart, and this is possible only at the cost of increasing the filling pressure of the heart Primary chronic inflammatory lung disease with a primary lesion of the distal respiratory tract and parenchyma, the formation of emphysema, impaired bronchial patency with the development of incompletely reversible or irreversible bronchial obstruction FEV 1 / FVC

With ardiopulmonary continuum CVD Death Risk factors Endothelial dysfunction Smoking Physical inactivity MS DM Smoking Physical inactivity MS DM Chronic inflammation COPD DN Ukena C, et al. The cardiopulmonary continuum systemic inflammation as common soil of heart and lung disease. Int J Cardiol 2010;145:172–176.

Aging physical inactivity Inflammation of lung tissue Weakness of skeletal muscles, cachexia Cardiovascular diseases IHD, CHF, AH Metabolic disorders DM, MS, obesity Bone disorders: osteoporosis Boschetto P, et al. Link between chronic obstructive pulmonary disease and coronary artery disease: implication for clinical practice. Respirology 2012;17:422–431

Large airways: Inflammation Impaired MC clearance Remodeling Bronchial wall changes Activation of FR Bronchioles: Inflammation Smooth muscle spasm Hypersensitivity Remodeling Peribronchial fibrosis Elastic tissue rupture Decrease in alveoli area in COPD Inflammation Macrophages and monocytes Damage to the wall Loss of acini Collapse of alveoli Air traps, bullae Decreased gas exchange CHF CHF: interstitial edema Alveolar edema Hydrothorax Obstruction of bronchioles Cardiomegaly (lung tightness) Alveoli in CHF Insufficiency of pulmonary capillaries Interruption of the alveolar-capillary barrier Thickening of the walls of capillaries and alveoli Violation of gas exchange Decreased diffusion capacity

LV systolic and diastolic dysfunction Valvular malformations Pulmonary vascular injury Endothelial dysfunction Acidosis Increased pulmonary vascular resistance RV dilatation RV failure Pulmonary hypertension Hypoxia Vasoconstriction Inflammation Pulmonary artery atherosclerosis PA embolism Increased LA pressure LA dilatation Pulmonary venous hypertension Increased LA wedge pressure Interruption of pulmonary veolar-capillary barrier N. M. Hawkins, et al. European Heart Journal (2013) 34, 2795–2803

Genetic factors Identification of genetic predisposition to COPD and CVD (hypertension, dyslipidemia, coronary artery disease) A functional relationship has been established between several risk factors (LDL receptor) Several genes associated with susceptibility to COPD have been identified (CHRA3-5 or FAM13A9) there is no potential single gene candidate for both phenotypes COPD and CVD both multigenic diseases, relationship not established Zeller T, et al. Genomewide association studies in cardiovascular disease–an update Clin Chem 2012;58:92–103. Todd JL, et al. The state of genome-wide association studies in pulmonary disease: a new perspective. Am J Respir Crit Care Med 2011;184:873–880

Clinical study of the combination of COPD and CHF interaction between vascular and pulmonary insufficiency is studied based on registries, subgroup analysis no prospective studies examining the specific role of pulmonary comorbidity in the treatment and outcome of cardiovascular disease retrospective analysis of the use of statins and / or RAAS blockers - improvement of course and prognosis in COPD, the benefits of combining therapy are needed in large randomized controlled trials in patients with COPD - with and without overt cardiovascular disease

Prevalence, prognosis of CHF COPD 1-3% of the general population annual mortality of 5-7% median survival after hospitalization 2 years above stage II COPD 5-10% annual mortality of about 3% after hospitalization - 25% prognosis - may become the third leading cause deaths worldwide by 2020 N. M. Hawkins, et al. European Heart Journal (2013) 34, 2795–2803

The prevalence of the combination of COPD and CHF varies widely depending on the sample, age, diagnostic criteria 10-40% of patients with CHF have simultaneously COPD study with spirometry - COPD was diagnosed in 36% (532 hospitalized patients with CHF) 30% - prospective study with stable CHF In COPD - CHF frequency up to 20.9% of patients in intensive care units 20.5 and 17% in stable COPD (echocardiography in all patients, systolic dysfunction and 13.8%) Conclusions COPD is much more common than CHF in the general population, COPD potentially masked in a significant proportion of CHF patients Iversen KK, et al. Chronic obstructive pulmonary disease in patients admitted with heart failure. J Intern Med 2008;264:361–369. Boschetto P, et al. Occurrence and impact of chronic obstructive pulmonary disease in elderly patients with stable heart failure. Respirology 2013;18:125–130 Macchia A, et al. Unrecognized ventricular dysfunction in COPD. Eur Respir J 2012;39:51–58.

COPD prognosis predicts mortality in patients with CHF Bronchoobstruction is associated with worse survival One study examined the prognostic consequences of the combination of CHF and COPD (echocardiography and respiratory function, 83 of 405 elderly patients with COPD were diagnosed with CHF (20.5%). Patients with CHF have a double risk mortality compared with no CHF during follow-up with a mean duration of 4.2 years) Rusinaru D, et al. Impact of chronic obstructive pulmonary disease on long-term outcome of patients hospitalized for heart failure. Am J Cardiol 2008;101:353–358.

Definition Dyspnea is a feeling of shortness of breath, objectively accompanied by changes in its frequency, depth and rhythm. she was not)

"Language of shortness of breath" 1. Frequency 2. Exhalation 3. Shallow breathing 4. Work 5. Choking 6. Lack of air 7. Constriction 8. Heaviness to the end 3. I find it difficult to inhale, take a deep breath, shallow breathing 4. My breathing requires effort 5. I feel like I am suffocating, that my breathing stops 6. I am short of breath 7. My chest is tight, constricted 8. My breathing is heavy Simon P.M., et al., 1990

Complaints Anamnesis Examination "Pulmonary" "Heart" Choking, "whistling", cough with phlegm Pain, fear, weakness, dry cough, nocturnal Smoking, allergological, occupational, RF infection and atherosclerosis clinic Diffuse cyanosis, signs of emphysema, dry wheezing, osteoarthropathy Acrocyanosis , cardiomegaly, abnormal sounds, murmurs, moist rales

Radiographic evidence of pulmonary edema Feature Cardiogenic edema Non-cardiogenic edema Heart size Normal or enlarged Usually normal Vascular shadowing Normal or enlarged Normal Vascular distribution Uniform or inverted Normal Distribution of edema Uniform Spotted or peripheral Pleural effusion May Not always Peribronchial effusion Present Not always Septal lines Present Not always Air bronchogram » Not always Usually present

Survey. Evaluation of respiratory function in CHF Signs of restriction - a hallmark of CHF, reflecting cardiomegaly, weakness of the respiratory muscles, interstitial fibrosis An increase in LA contributes to the interruption of the interaction between the structure and function of capillaries An increase in pressure in the pulmonary capillaries contributes to the activation of growth factors, thickening of the alveolar-capillary barrier and modeling of the vessel wall Diffusion decreases gases through this barrier Pulmonary hypertension - further contributes to RV type HF Signs of obstruction - may be typical of pulmonary edema due to bronchial obstruction by edematous interstitial tissue, increased bronchial reactivity FEV 1 improves during diuretic therapy up to normal numbers

Survey. ECHO CS There may be a poor “US window” Identification of the etiology of CHF Evaluation of contractility Prevalence of changes in the left heart in the presence of PH Prevalence of dilatation of the right parts and PH in COPD Pulmonary artery pressure higher pressure figures in the combination of COPD and CHF (about 50 mm Hg. Art. .) than in COPD (about 30 mmHg)

Survey. BNP False positive test: Increased in PAH pancreatic insufficiency Lung diseases Decreases specificity for CHF Bozkanat E, et al. The significance of elevated brain natriuretic peptide levels in chronic obstructive pulmonary disease. J Int Med Res 2005;33:537–544. Rutten FH, et al. Comparison of B-type natriuretic peptide assays for identifying heart failure in stable elderly patients with a clinical diagnosis of chronic obstructive pulmonary disease. Eur J Heart Fail 2007;9:651–659.

Example. A 62-year-old man Smoker for about 30 years, continues to smoke about a pack a day 5 years ago suffered from MI, took drugs only for the first year, then nothing bothered him, stopped taking all drugs Complaints of shortness of breath with previously well tolerated loads ): diffuse cyanosis, moderate acrocyanosis, on percussion a box sound over the lungs, cardiomegaly (displacement of the OCT border to the left), on auscultation - weakened breathing, single dry rales during forced expiration, the 1st tone is equal to the second at the apex

"Cardiac drugs" for COPD should NOT Worse bronchial patency Cause hypokalemia (impairs the function of the respiratory muscles, progression of DN) Decrease BCC Increase platelet aggregation Provoke the development of cough Weaken the effects of basic bronchodilator therapy Increase pressure in the pulmonary artery Deteriorate endothelial function

Candesartan (Atakand) Indications for use: Arterial hypertension Chronic heart failure Contraindications for use: Hypersensitivity to candesartan cilexetil or other components that make up the drug Pregnancy and lactation Instructions for use of the drug Atakand, Atakand Plus

Competitive and non-competitive AT 1 receptor antagonists According to the nature of the interaction with the angiotensin II receptor, they are distinguished Competitive (losartan, eprosartan) Non-competitive (valsartan, irbesartan, candesartan, telmisartan) provide stronger and longer binding to the angiotensin II receptor

Excretion route Hepatic elimination (%) Renal excretion (%) Losartan Valsartan Irbesartan Candesartan cilexitil Telmisartan Eprosartan No dose adjustment necessary in patients with mild to moderate renal and hepatic impairment

Candesartan (Atacand): pharmacokinetic profile Half-life (t 1/2) ~ 9 hours Does not accumulate with prolonged use Food intake does not have a significant effect No clinically significant pharmacokinetic interactions No need to adjust the dose in patients with mild to moderate impaired renal and hepatic function Instructions on the use of the drug Atakand, Atakand Plus

Combination of beta-blockers and beta-agonists Opposite pharmacological effects Depends on selectivity Non-selective beta-blockers are antagonists of beta-2 mediated vasodilation Response to beta-agonists depends on beta-blockers Need research to investigate this clinical interaction? Bristow MR, et al. Beta 1- and beta 2-adrenergic-receptor subpopulations in nonfailing and failing human ventricular myocardium: coupling of both receptor subtypes to muscle contraction and selective beta 1-receptor down-regulation in heart failure. Circ Res 1986;59:297–309. Packer M. Pathophysiologicalmechanisms underlying the effects of beta-adrenergic agonists and antagonists on functional capacity and survival in chronic heart failure. Circulation 1990;82:I77–188

Diuretics in CHF Indicated in the presence of fluid retention syndrome: Shortness of breath, fatigue, weakness, lack of appetite Edema, jugular vein pulsation, moist rales, hepatomegaly, ascites, hypervolemia, cachexia to strong, from monotherapy to combination

Exacerbation of COPD and CHF Clinical manifestations of fluid stasis and bronchial obstruction The presence of symptoms of volume overload (edema, jugular venous pulsation, moist rales, hepatomegaly, ascites, hypervolemia, cachexia) - predictive value in favor of AHF - from 2 to 11 times predictive value in favor of AHF 5.8 times High predictive value of negative BNP

Estimation of the severity of stagnation (in points) Indicator 0123 Orthopnoenet mild moderate severe CVP (cm) Less than More than 16 hepatomegaly no edge Moderate pulsation Pronounced increase in edema /4+ BNP Less than More than 500 NT-proBNP Less than More than 3000 change Т 6 МХMore than 400 m Less than 100

Diuretics for AHF Furosemide IV mg Dose at least equivalent to oral High doses (greater than 200 mg) Worse kidney function Do not reduce risk of hospitalization Worse mortality

For citation: Akhmetzyanova E.Kh., Gainitdinova V.V., Sharafutdinova L.A. Management of patients with chronic heart failure with preserved systolic function against the background of severe COPD in the acute phase // BC. 2014. No. 2. S. 138

Currently, the goals of the treatment of heart failure (HF), according to the recommendations of the European Society of Cardiology (ESC, 2012) for the diagnosis and treatment of acute and chronic heart failure (CHF), are to reduce symptoms and manifestations, prevent hospitalization and improve survival. The treatment strategy includes: drugs indicated in potentially all patients with symptomatic (FC II-IV NYNA) HF (ACE inhibitors, β-blockers, APM), and drugs with less efficacy in patients with symptomatic (FC II-IV NYNA) HF ( ARB, ivabradine, digoxin, isosorbide dinitrate, omega-3-PUFA). The results of the SHIFT study conducted in 2010 showed that elevated heart rate is a marker of an adverse outcome of CHF and proved that the concept of neurohormonal blockade in CHF can be supplemented by effective heart rate reduction with the β-channel blocker ivabradine.

Of interest is a new therapeutic approach in the treatment of CHF, which is based on the effective control of heart rate through the use of the inhibitor of if-channels ivabradine, recently included in the treatment of CHF in patients with sinus rhythm, ejection fraction (EF) ≤35%, heart rate ≥70 beats. ./min., persistent symptoms (FC II-III NYNA) with intolerance to β-blockers.

The SHIFT study also demonstrated a reduction in the relative risk for the primary combined outcome of cardiovascular death or hospitalization for heart failure, improved LV function and quality of life with ivabradine treatment.

In Russia, chronic obstructive pulmonary disease (COPD) as the cause of CHF, according to the Society of Heart Failure Specialists (OSSN, 2010), is noted in 13% of cases. Diagnosis of heart failure in COPD presents certain difficulties, since it is largely masked by manifestations of acute and chronic respiratory failure. Treatment of COPD, according to the global initiative GOLD 2011, 2013, includes the appointment of bronchodilators (short- and long-acting β2-agonists, short- and long-acting M-anticholinergics, methylxanthines), inhaled glucocorticosteroids (IGCS), combined long-acting β2-agonists + ICS , systemic corticosteroids (not recommended for long-term use), phosphodiesterase IV inhibitors (for GOLD III, GOLD IV). With exacerbation, antibiotics, mucolytics, oxygen therapy are prescribed.

Patients with HF receiving inhaled β2-agonists have an increased risk of death and hospitalization, according to an observational study, which probably indicates the need for more careful monitoring of patients with severe HF receiving inhaled β2-agonists for COPD.

Calcium channel blockers in this category of patients can exacerbate congestive heart failure and lead to the appearance of peripheral edema.

Therapy with selective β1-blockers has a significant impact on the survival of patients with HF, and the presence of COPD is the most important reason why this category of patients does not receive full treatment.

Treatment of patients with combined pathology always presents certain difficulties; Thus, attempts at active drug treatment of one disease are associated with a real threat of iatrogenic exacerbation of concomitant pathology.

A study was made of the effect of the If-channel inhibitor ivabradine on the clinical symptoms of CHF in patients with severe COPD in the exacerbation phase.

Materials and methods

The study included 120 patients with CHF syndrome in severe COPD in the acute phase. COPD was diagnosed according to the 2010 GOLD guidelines, CHF syndrome was established according to the ESC Guidelines for CHF (2012) based on 4 criteria: typical symptoms, typical signs, normal LV EF and structural and functional changes in the heart (LA expansion, LV diastolic dysfunction ).

Criteria for inclusion in the study:

1. COPD (GOLD III, GOLD IV, 2010), exacerbation phase.

2. Sinus rhythm (heart rate above 70 bpm).

3. Pulmonary hypertension (above 20 mm Hg at rest).

4. Chronic cor pulmonale.

6. Informed consent of the patient to participate in the study.

Criteria for exclusion from the study:

1. Acute forms of cardiovascular disease (acute coronary syndrome, acute myocardial infarction, acute cerebrovascular accident).

1. Chronic form of atrial fibrillation.

2. Paroxysmal arrhythmias.

3. Diabetes.

All patients initially, after 1 and 3 weeks. ECG was performed at rest, heart rate was determined. Echocardiography was performed (at the same time intervals) using the Fillips NNVVISERCHD device - standard hemodynamic parameters were studied, the size of the left ventricle in diastole (VDR LV), the size of the left ventricle in systole (VDR LV), end diastolic volume of the left ventricle (EDV LV), final left ventricular systolic volume (LV systolic volume), stroke volume (SV), left ventricular ejection fraction (LV EF), left atrium (LA), right atrium (RA), right ventricular wall thickness (RV TS), right ventricular end-diastolic size in diastole (KDRd RV), systolic pressure in the pulmonary artery (Ppa), the ratio of the E / A velocities of the LV and RV. To study the function of external respiration (RF), computer spirometry was performed using the Master Screen Body (Jaeger), the indicators of forced expiratory volume in the first second (FEV1), forced vital capacity (FVC), and the ratio of FEV1/FVC were studied. Daily self-monitoring of blood pressure (SBP) was carried out using the Digital Automatic Blood Pressure Monitor M4 (Omron) with registration of heart rate. Exercise tolerance was assessed using a 6-minute step test followed by an assessment of the severity of dyspnea according to Borg, the assessment of the clinical condition in CHF was carried out on the SHOKS scale initially, after 1 and 3 weeks, blood oxygen saturation (SaO2) was determined before and after exercise using an MD300C finger pulse oximeter at the same time intervals.

Statistical data processing was performed using the STATISTICA V.6.0 software package (StatsoftInc, USA). Average statistics are obtained: arithmetic mean with an error of the arithmetic mean. Friedman ANOVA, non-parametric Wilcoxon matchedpairs test, Spearman's non-parametric correlation analysis (r), and two-factor analysis of variance were used. The null hypothesis about the absence of group differences was rejected at p<0,05.

Results and discussion

The study included patients who were treated in the intensive care and pulmonology departments of the Republican Clinical Hospital. G.G. Kuvatov (Ufa) regarding the treatment of COPD exacerbation. All patients had a history of COPD with an average duration of the disease of 12.84±0.53 years, and in the last 1-2 years there was a progression of deterioration in the general condition, dyspnea increased, according to medical records, repeated (≥2) hospitalizations were recorded over the past year . 12.5% ​​of patients were treated in the intensive care unit (4.5±1.21 days on average). Among comorbidities, 24.1% of patients had ischemic heart disease, stable exertional angina of functional class II (FC), myocardial infarction (MI), 17.5% had arterial hypertension (AH) of I-II degree. Diagnostic and sanitation fibrobronchoscopy was performed in 109 (72.67%) patients.

The test with physical activity (6-minute walking test) was carried out on the 1st-2nd day. upon admission to the pulmonology department or after transfer from the intensive care unit. The clinical characteristics of the patients included in the study are presented in Table 1.

In patients, complaints of cough with the release of difficult-to-separate mucous and mucopurulent sputum, and shortness of breath at rest prevailed. Shortness of breath of varying severity was observed in all patients: in 75% of cases it manifested itself as a feeling of lack of air, in 12.5% ​​- in the form of suffocation, in 95.8% - in the form of shortness of breath with little physical exertion, in 26.6% - in the form of shortness of breath at rest. About half of the patients (46.6%) complained of pain and discomfort in the region of the heart. Palpitations, interruptions in the work of the heart were noted by the vast majority of patients - in 84.2% of cases. The patients also complained of general weakness, increased fatigue, and edema of the lower extremities (Table 2).

During an objective examination, acrocyanosis was observed in 56.6% of the examined patients, in 25% of patients there were phenomena of diffuse cyanosis. Dry wheezing rales were heard in all patients. The average frequency of respiratory movements was 23.50±1.26 per minute; a decrease in blood oxygen saturation (SaO2) to 90.74±0.69% was recorded.

The severity of dyspnea, assessed using the mMRC questionnaire, averaged 3.09±0.03 points. Increased heart rate was observed in all patients, averaging 101.02±0.81 bpm. Emphasis of tone II on the pulmonary artery was detected during auscultation in patients in 75.8% of cases. The average systolic blood pressure (SBP) was 119.31 ± 1.41 mm Hg. Art., diastolic blood pressure (DBP) - 68.34±0.77 mm Hg. Art. When assessing the clinical condition on the SHOKS scale and the distance of the 6-minute walking test, CHF syndrome corresponded to functional class III (Table 3).

An increase in the size of the liver and the presence of peripheral edema were noted in 25 (25.8%) patients.

Echocardiographic parameters of the heart in the studied patients were characterized by an increase in RV TPS, a decrease in the E/A ratio of the right ventricle, and an increase in the systolic pressure in the pulmonary artery. Along with changes in the right parts of the heart, pathological structural and functional changes in the left parts of the heart were noted. There was a slight increase in the average size of the left atrium up to 35.12±0.30 mm, which indirectly indicates an increase in filling pressure and a decrease in the function of the left ventricle (LV). Violations of LV systolic function (decrease in EF less than 50%) were not detected in any of the observed cases, the average values ​​of LV EF approached the upper limit of normal and reached 64.28±0.43%. LV diastolic dysfunction was recorded in 87.33% of patients, manifested by a decrease in the E/A ratio. The predominant type of LV diastolic dysfunction was relaxation. In 5 (3.3%) patients with an extremely severe course, a pseudonormal type of LV filling was observed.

All patients with COPD received standard therapy (GOLD 2011, 2013): bronchodilators (tiotropium bromide or its combination with long-acting β2-agonists), inhaled (IGCS) and systemic (SGCS) glucocorticoids, antibiotics, mucolytics. CHF was treated with mineralocorticoid receptor (ARM) antagonists - spironolactone 50-75 mg/day, angiotensin-converting enzyme (ACE) inhibitors - enalapril at a dose of 5-10 mg/day, or angiotensin receptor blockers (ARBs) valsartan at a dose of 40 mg/day. β-blockers were not prescribed due to the pronounced broncho-obstructive component in the observed patients, associated with the severity of the disease and the exacerbation phase.

The patients were divided into two groups: a comparison group of 60 people and a study group of 60 people. The groups were formed by random sampling, did not differ statistically significantly (p>0.05) in age, gender, clinical characteristics, baseline heart rate, standard therapy, and therefore were regarded as identical. Each group had the same number of patients with concomitant pathology of the cardiovascular system. Groups were randomized to receive ivabradine (titrated to a maximum dose of 7.5 mg 2 times a day) or standard treatment for COPD in the acute phase (GOLD 2011, 2013). Dynamic observation was carried out for 18 days.

When comparing the initial clinical and instrumental parameters in the studied groups, no statistically significant differences were observed in any case (p>0.05). Most of the patients had a reduced level of blood oxygenation. The respiratory rate in patients of both groups was 22.40±1.08 and 23.62±1.14 bpm. respectively. Sinus tachycardia was recorded in both groups, heart rate was 99.46±7.99 in the comparison group and 102.53±13.59 bpm. - in the study group. In most patients, according to the results of the test with a 6-minute walk, CHF FC III (according to NYHA) was established.

In the study of hemodynamic parameters in the comparison and study groups, an increase in the wall thickness of the right ventricle 6.0 ± 0.35 mm and 6.03 ± 0.35 mm, respectively, an increase in the level of mean pressure over the pulmonary artery to 38.0 ± 2.8 mm was observed rt. Art. and 39.15±2.46 mm Hg. Art., decrease in peak velocities E/A of the left ventricle. The LV systolic function in all groups was intact, the mean values ​​of LV EF approached the upper limit of normal and amounted to 63.64±1.02% and 62.35±1.61%, respectively. The data of our work are consistent with the results of N.A. Karoli, R. Yilmaz, M. Gencer, E. Ceylan, R.U. Demirbag. Left ventricular diastolic dysfunction manifested itself as a decrease in the ratio of LV E/A peaks and was detected in 73.0% of all patients studied. The predominant type of LV diastolic dysfunction was relaxation.

The diagram of the distribution of heart rate in the studied patients (Fig. 1) clearly shows that the most frequent heart rate was recorded in the range from 90 to 100 bpm. There were no differences in heart rate in severe and extremely severe COPD (p>0.25).

In patients treated with ivabradine, the drug was well tolerated. During the entire observation period, no side effects were registered in any case, none of the patients noted an increase in cough, shortness of breath, or the appearance of respiratory discomfort.

The assessment of the clinical condition in CHF in patients with COPD in both groups improved during treatment. Statistically significant differences between the groups were obtained according to the results of the SHOKS scale; against the background of standard treatment, there was a decrease in SHOKS to 5.25±0.18 points, against the background of ivabradine - to 4.09±0.18 points. The additional appointment of ivabradine led to an improvement in the clinical condition in patients with CHF during exacerbation of severe and extremely severe COPD (p<0,05) (рис. 2).

According to diary entries, the majority of patients in the study group noted a subjective improvement in their condition and exercise tolerance. After 3 weeks treatment, patients showed an increase in exercise tolerance, which manifested itself in a statistically significant increase in the distance traveled and a decrease in dyspnea on the Borg scale (p<0,05), по сравнению с данными группы сравнения (рис. 3).

Against the background of standard treatment, the distance traveled in 6 min. increased by 14.49% (from 237.05 to 277.23 m), against the background of the appointment of ivabradine - by 22.58% (from 236.25 to 305.48 m) (p<0,05) (рис. 4).

In all patients of the comparison groups and study groups during treatment (Fig. 5), a statistically significant decrease in heart rate was recorded (p< 0,05). Но снижение ЧСС до целевых величин (ЧСС < 70 уд./мин., ВНОК 2010 г.) было достигнуто только при назначении ивабрадина в дозе 15 мг/сут независимо от исходной ЧСС. При назначении ивабрадина в дозе 10 мг/сут снижение ЧСС наблюдалось на 4-5-й день приема препарата, целевого уровня ЧСС достичь не удалось. На фоне приема ивабрадина в дозе 15 мг/сут снижение ЧСС уже со 2-го дня приема препарата отмечалось у 92% больных, но статистически значимое снижение ЧСС наблюдалось через 2 нед. от начала лечения (p <0,001).

In order to study the dependence of the effectiveness of ivabradine in patients with severe and extremely severe COPD with CHF syndrome on the initial heart rate, a multivariate analysis of variance was performed. The analysis included two factors: heart rate (two categories - less than 100 bpm, more than 100 bpm) and treatment with ivabradine (two categories - before and after treatment). For this, the study group, taking into account the distribution of initial heart rate values ​​(Fig. 1), was divided into 2 subgroups: with heart rate<100 уд./мин. и ЧСС >100 bpm (Fig. 6, 7). The results of the analysis showed no dependence of the effectiveness of treatment with ivabradine on the initial heart rate in the studied patients.

When analyzing the influence of factors on exercise tolerance, an improvement in the indicator was noted during treatment with ivabradine, regardless of the initial heart rate (Fig. 6).

Thus, two-way analysis indicates the significance of the effect of ivabradine on the results of a 6-minute step test.

Analysis of the influence of two factors (heart rate and treatment with ivabradine) on the assessment of the clinical state in CHF SHOKS in the studied patients also showed that the positive effect of ivabradine in sinus tachycardia does not depend on the initial heart rate (Fig. 7).

Analysis of the influence of two factors (heart rate and treatment with ivabradine) on the severity of dyspnea according to the Borg questionnaire in the studied patients showed that the positive effect of ivabradine depends on the initial heart rate. In patients with baseline heart rate >100 beats/min. there was a greater degree of reduction in dyspnea, assessed by this questionnaire (p<0,05).

Thus, the improvement in the assessment of the clinical condition in CHF according to the SHOKS scale and the increase in exercise tolerance in CHF patients with severe COPD in the exacerbation phase during treatment with ivabradine do not depend on the initial heart rate. The effectiveness of treatment with ivabradine is the same both with a heart rate of 70 to 100 bpm and with severe tachycardia. The decrease in dyspnea according to the Borg questionnaire during treatment with ivabradine is more pronounced in patients with a heart rate >100 bpm.

conclusions

1. In patients with severe and extremely severe COPD, the duration of the disease for more than 10 years, CHF is recorded with preserved systolic function of the left ventricle.

2. The inclusion of ivabradine in the complex treatment of patients with CHF during exacerbation of severe COPD leads to an improvement in the clinical condition: a decrease in CHF symptoms, a statistically significant increase in exercise tolerance, an increase in functional ability, and a decrease in the severity of dyspnea. A decrease in dyspnea according to the Borg questionnaire during treatment with ivabradine is more pronounced in patients with an initial heart rate of >100 bpm.

3. Ivabradine at a dose of 15 mg/day can be recommended for the management of CHF patients with preserved systolic function in severe COPD in the acute phase.

Chronic obstructive pulmonary disease or COPD refers to chronic lung diseases associated with respiratory failure. Bronchial damage develops with emphysema complications against the background of inflammatory and external stimuli and has a chronic progressive character.

The alternation of latent periods with exacerbations requires a special approach to treatment. The risk of developing serious complications is quite high, which is confirmed by statistical data. Respiratory dysfunction causes disability and even death. Therefore, patients with this diagnosis need to know COPD, what it is and how the disease is treated.

general characteristics

When exposed to the respiratory system of various irritating substances in people with a predisposition to pneumonia, negative processes begin to develop in the bronchi. First of all, the distal sections are affected - located in close proximity to the alveoli and lung parenchyma.

Against the background of inflammatory reactions, the process of natural discharge of mucus is disturbed, and small bronchi are clogged. When an infection is attached, inflammation spreads to the muscle and submucosal layers. As a result, bronchial remodeling occurs with replacement by connective tissues. In addition, lung tissue and bridges are destroyed, which leads to the development of emphysema. With a decrease in the elasticity of the lung tissues, hyperairiness is observed - the air literally inflates the lungs.

Problems arise precisely with the exhalation of air, since the bronchi cannot fully expand. This leads to a violation of gas exchange and a decrease in the volume of inhalation. A change in the natural process of breathing manifests itself in patients as shortness of breath in COPD, which is greatly enhanced by exertion.

Persistent respiratory failure causes hypoxia - oxygen deficiency. All organs suffer from oxygen starvation. With prolonged hypoxia, the pulmonary vessels narrow even more, which leads to hypertension. As a result, irreversible changes in the heart occur - the right section increases, which causes heart failure.

Why is COPD classified as a separate group of diseases?

Unfortunately, not only patients, but also medical workers are poorly informed about such a term as chronic obstructive pulmonary disease. Doctors habitually diagnose emphysema or chronic bronchitis. Therefore, the patient does not even realize that his condition is associated with irreversible processes.

Indeed, in COPD, the nature of symptoms and treatment in remission are not much different from the signs and methods of therapy for pulmonary pathologies associated with respiratory failure. What then made physicians single out COPD as a separate group.

Medicine has determined the basis of such a disease - chronic obstruction. But the narrowing of the gaps in the airways are also found in the course of other pulmonary diseases.

COPD, unlike other diseases such as asthma and bronchitis, cannot be permanently cured. Negative processes in the lungs are irreversible.

So, in asthma, spirometry shows improvement after bronchodilators are used. Moreover, the indicators of PSV, FEV may increase by more than 15%. While COPD does not provide significant improvements.

Bronchitis and COPD are two different diseases. But chronic obstructive pulmonary disease can develop against the background of bronchitis or proceed as an independent pathology, just like bronchitis can not always provoke COPD.

Bronchitis is characterized by a prolonged cough with sputum hypersecretion and the lesion extends exclusively to the bronchi, while obstructive disorders are not always observed. Whereas sputum separation in COPD is not increased in all cases, and the lesion extends to structural elements, although bronchial rales are auscultated in both cases.

Why does COPD develop?

Not so few adults and children suffer from bronchitis, pneumonia. Why, then, chronic obstructive pulmonary disease develops only in a few. In addition to provoking factors, predisposing factors also affect the etiology of the disease. That is, the impetus for the development of COPD can be certain conditions in which people who are prone to pulmonary pathologies find themselves.

Predisposing factors include:

1. hereditary predisposition. It is not uncommon to have a family history of certain enzyme deficiencies. This condition has a genetic origin, which explains why the lungs do not mutate in a heavy smoker, and COPD in children develops for no particular reason.
2. Age and gender. For a long time it was believed that pathology affects men over 40. And the rationale is more related not to age, but to smoking experience. But today the number of women who smoke with experience is no less than that of men. Therefore, the prevalence of COPD among the fair sex is no less. In addition, women who are forced to breathe cigarette smoke also suffer. Passive smoking negatively affects not only the female, but also the children's body.
3. Problems with the development of the respiratory system. Moreover, we are talking about both the negative impact on the lungs during intrauterine development, and the birth of premature babies whose lungs did not have time to develop for full disclosure. In addition, in early childhood, the lag in physical development negatively affects the state of the respiratory system.
4. Infectious diseases. With frequent respiratory diseases of infectious origin, both in childhood and at an older age, it increases the risk of developing COL at times.
5. Hyperreactivity of the lungs. Initially, this condition is the cause of bronchial asthma. But in the future, the addition of COPD is not ruled out.

But this does not mean that all patients at risk will inevitably develop COPD.

Obstruction develops under certain conditions, which can be:

1. Smoking. Smokers are the main patients diagnosed with COPD. According to statistics, this category of patients is 90%. Therefore, it is smoking that is called the main cause of COPD. And the prevention of COPD is based primarily on smoking cessation.
2. Harmful working conditions. People who, by the nature of their work, are forced to regularly inhale dust of various origins, air saturated with chemicals, and smoke suffer from COPD quite often. Work in mines, construction sites, in the collection and processing of cotton, in metallurgical, pulp, chemical production, in granaries, as well as in enterprises producing cement, other building mixtures leads to the development of respiratory problems to the same extent in smokers and non-smokers .
3. Inhalation of combustion products. We are talking about biofuels: coal, wood, manure, straw. Residents who heat their homes with such fuel, as well as people who are forced to be present during natural fires, inhale combustion products that are carcinogens and irritate the respiratory tract.

In fact, any external effect on the lungs of an irritating nature can provoke obstructive processes.

Main complaints and symptoms

The primary signs of COPD are associated with coughing. Moreover, cough, to a greater extent, worries patients in the daytime. At the same time, sputum separation is insignificant, wheezing may be absent. The pain practically does not bother, sputum leaves in the form of mucus.

Sputum with the presence of pus or a cough that provokes hemoptysis and pain, wheezing - the appearance of a later stage.

The main symptoms of COPD are associated with the presence of shortness of breath, the intensity of which depends on the stage of the disease:

• With mild shortness of breath, breathing is forced against the background of fast walking, as well as when climbing a hill;
• Moderate shortness of breath is indicated by the need to slow down the pace of walking on a flat surface due to breathing problems;
• Severe shortness of breath occurs after several minutes of walking at a free pace or walking a distance of 100 m;
• For shortness of breath of the 4th degree, the appearance of breathing problems during dressing, performing simple actions, immediately after going out into the street is characteristic.

The occurrence of such syndromes in COPD may accompany not only the stage of exacerbation. Moreover, with the progress of the disease, the symptoms of COPD in the form of shortness of breath, cough become stronger. On auscultation, wheezing is heard.

Breathing problems inevitably provoke systemic changes in the human body:

• The muscles involved in the breathing process, including the intercostal ones, atrophy, which causes muscle pain and neuralgia.
• In the vessels, changes in the lining, atherosclerotic lesions are observed. Increased tendency to form blood clots.
• A person is faced with heart problems in the form of arterial hypertension, coronary disease and even a heart attack. For COPD, the pattern of cardiac changes is associated with left ventricular hypertrophy and dysfunction.
• Osteoporosis develops, manifested by spontaneous fractures of the tubular bones, as well as the spine. Constant joint pain, bone pain cause a sedentary lifestyle.

The immune defense is also reduced, so any infections are not rebuffed. Frequent colds, in which there is a high temperature, headache, and other signs of an infectious lesion, are not a rare picture in COPD.

There are also mental and emotional disorders. Working capacity is significantly reduced, a depressive state, unexplained anxiety develops.

It is problematic to correct emotional disorders that have arisen against the background of COPD. Patients complain of apnea, stable insomnia.

In the later stages, cognitive disorders also appear, manifested by problems with memory, thinking, and the ability to analyze information.

Clinical forms of COPD

In addition to the stages of development of COPD, which are most often used in medical classification,

There are also forms of the disease according to the clinical manifestation:

1. bronchial type. Patients are more likely to cough, wheezing with sputum discharge. In this case, shortness of breath is less common, but heart failure develops more rapidly. Therefore, there are symptoms in the form of swelling and cyanosis of the skin, which gave the name to the patients "blue edema".
2. emphysematous type. The clinical picture is dominated by shortness of breath. The presence of cough and sputum is rare. The development of hypoxemia and pulmonary hypertension is observed only in the later stages. In patients, the weight decreases sharply, and the skin becomes pink-gray, which gave the name - "pink puffers".

However, it is impossible to speak of a clear division, since in practice COPD of a mixed type is more common.

Exacerbation of COPD

The disease can be aggravated unpredictably under the influence of various factors, including external, irritating, physiological and even emotional. Even after eating in a hurry, choking may occur. At the same time, the condition of a person is deteriorating rapidly. Increasing cough, shortness of breath. The use of the usual basic COPD therapy in such periods does not give results. During the period of exacerbation, it is necessary to adjust not only the methods of COPD treatment, but also the doses of the drugs used.

Usually, treatment is carried out in a hospital, where it is possible to provide emergency assistance to the patient and conduct the necessary examinations. If exacerbations of COPD occur frequently, the risk of complications increases.

Urgent Care

Exacerbations with sudden attacks of suffocation and severe shortness of breath must be stopped immediately. Therefore, emergency assistance comes to the fore.

It is best to use a nebulizer or spacer and provide fresh air. Therefore, a person predisposed to such attacks should always have inhalers with them.

If first aid does not work and suffocation does not stop, it is urgent to call an ambulance.

Video

Chronic obstructive pulmonary disease

Principles of treatment for exacerbations

• Short bronchodilators are used with an increase in the usual dosages and frequency of administration.
• If bronchodilators do not have the desired effect, Eufilin is administered intravenously.
• It can also be prescribed for exacerbation of COPD treatment with beta-stimulants in combination with anticholinergic drugs.
• If pus is present in the sputum, antibiotics are used. Moreover, it is advisable to use antibiotics with a wide spectrum of action. It makes no sense to use narrowly targeted antibiotics without bakposev.
• The attending physician may decide to prescribe glucocorticoids. Moreover, Prednisolone and other drugs can be prescribed in tablets, injections or used as inhaled glucocorticosteroids (IGCS).
• If oxygen saturation is significantly reduced, oxygen therapy is prescribed. Oxygen therapy is carried out using a mask or nasal catheters to ensure proper oxygen saturation.

In addition, drugs can be used to treat diseases that frolic against the background of COPD.

Basic treatment

To prevent seizures and improve the general condition of the patient, a set of measures is taken, among which behavioral and drug treatment, dispensary observation is not the last.

The main drugs used at this stage are bronchodilators and corticosteroid hormones. Moreover, it is possible to use long-acting bronchodilator drugs.

Together with taking medications, it is necessary to pay attention to the development of pulmonary endurance, for which breathing exercises are used.

As for nutrition, the emphasis is on getting rid of excess weight and saturation with the necessary vitamins.

The treatment of COPD in the elderly, as well as in severe patients, is associated with a number of difficulties due to the presence of concomitant diseases, complications and reduced immune protection. Often such patients require constant care. Oxygen therapy in such cases is used at home and, at times, is the main way to prevent hypoxia and related complications.

When the damage to the lung tissue is significant, cardinal measures are necessary with resection of a part of the lung.

Modern methods of cardinal treatment include radiofrequency ablation (ablation). It makes sense to do RFA when detecting tumors, when for some reason the operation is not possible.

Prevention

The main methods of primary prevention directly depend on the habits and lifestyle of a person. Smoking cessation, the use of personal protective equipment significantly reduces the risk of developing lung obstruction.

Secondary prevention is aimed at preventing exacerbations. Therefore, the patient must strictly follow the recommendations of doctors for treatment, as well as exclude provoking factors from their lives.

But even cured, operated patients are not fully protected from exacerbations. Therefore, tertiary prevention is also relevant. Regular medical examination allows you to prevent the disease and detect changes in the lungs in the early stages.

Periodic treatment in specialized sanatoriums is recommended for both patients, regardless of the stage of COPD, and cured patients. With such a diagnosis in the anamnesis, vouchers to the sanatorium are provided on a preferential basis.